Effects of C/EBPα overexpression on alveolar epithelial type II cell proliferation, apoptosis and surfactant protein-C expression after exposure to hyperoxia

BACKGROUND: This study aims to investigate the effects of CCAAT/enhancer binding protein alpha (C/EBPα) overexpression on cell proliferation, apoptosis and surfactant protein-C(SP-C) in alveolar epithelial type II (AEC II) cells after exposure to hyperoxia. METHODS: pcDNA3.1(+)-C/EBPα plasmid or air-empty vector were transfected into AEC II cells with or without hyperoxia. AEC II cells were divided into air group, air+pcDNA3.1-C/EBPα group, air-empty vector group, hyperoxia group, hyperoxia+pcDNA3.1-C/EBPα group, and hyperoxia-empty vector group. Cell proliferation was analyzed using Cell Counting Kit-8. The mRNA level and protein expression were measured using PCR and Western blot techniques, respectively. The cell cycle and apoptosis were analyzed using flow cytometry. RESULTS: After 48 h of post-transfection, significantly higher protein expression of C/EBPα was observed in the C/EBPα transfection group with or without hyperoxia compared to the others (P < 0.05). Compared to the air group, hyperoxia decreased cell proliferation, increased apoptosis, decreased SP-C expression, decreased percentage of cells in G1 phase, and increased percentage of cells in the S and G2 phases (P < 0.05); however, reversed by C/EBPα transfection (P < 0.05). No significant changes were observed in cell proliferation, SP-C expression, and apoptosis rates in the C/EBPα transfection group as compared to the controls air-empty vector group. CONCLUSION: C/EBPα overexpression significantly upregulates the expression of SP-C, promotes cell proliferation, and inhibits apoptosis in AEC II cells after exposure to hyperoxia. Hence, this data suggests that C/EBPα overexpression may reverse the damage and exert a protective role in hyperoxia-induced lung injury. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12890-019-0911-x) contains supplementary material, which is available to authorized users.